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Epigenetic regulation of the inflammatory response in stroke

Neural Regeneration research 2025年第11期20卷 3045-3062页

作者： Jingyi Liang Fei Yang Zixiao Li Qian Li School of Basic Medical Sciences Capital Medical UniversityBeijingChina Department of Neurobiology School of Basic Medical SciencesCapital Medical UniversityBeijingChina laboratory for Clinical medicine Beijing Key Laboratory of Neural Regeneration and RepairCapital Medical UniversityBeijingChina Department of Neurology Beijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical research Center for Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina National Center for Healthcare quality Management in Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina chinese Institute for Brain research BeijingChina research Unit of Artificial Intelligence in Cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina Beijing Engineering research Center of Digital Healthcare for Neurological Diseases BeijingChina Department of Biochemistry and Molecular Biology School of Basic Medical SciencesCapital Medical UniversityBeijingChina Beijing key laboratory of Cancer Invasion and Metastasis research Capital Medical UniversityBeijingChina

Stroke is classified as ischemic or hemorrhagic,and there are few effective treatments for either *** mechanisms play a critical role in secondary brain injury following a stroke,which manifests as cytokine release,blood–brain barrier disruption,neuronal cell death,and ultimately behavioral *** the inflammatory response has been shown to mitigate this cascade of events in experimental stroke ***,in clinical trials of anti-inflammatory agents,longterm immunosuppression has not demonstrated significant clinical benefits for *** may be attributable to the dichotomous roles of inflammation in both tissue injury and repair,as well as the complex pathophysiologic inflammatory processes in *** acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic *** agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of ***,epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke *** this review,we summarize current findings on the epigenetic regulation of the inflammatory response in stroke,focusing on key signaling pathways including nuclear factor-kappa B,Janus kinase/signal transducer and activator of transcription,and mitogen-activated protein kinase as well as inflammasome *** also discuss promising molecular targets for stroke *** evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke,leading to improved post-stroke outcomes.

关键词： DNA methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding RNA RNA methylation subarachnoid hemorrhage treatment

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Essential Role of chinese medicines in Mesenchymal Stem Cells Transplantation for Treatment of Ischemic Stroke

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chinese Journal of Integrative medicine 2019年第10期25卷 723-727页

作者： ZHAO Yong-hua state key laboratory of quality research in chinese medicine Institute of Chinese Medical Sciences University of Macao

Ischemic stroke accounts for the majority of all strokes and has been primary causes of long-term disability and mortality in worldwide. Mesenchymal stem cell(MSC) therapy suggests significantly improved effects on neurological functional outcome, neurogenesis, angiogenesis, blood-brain barrier permeability, inflammatory injury, neuroprotection and so on, following stroke. However, the occurrence of adverse effects results in restriction of the therapy. chinese medicine accumulates abundant clinical experiences on stroke for over two thousand years, and some formulae and active ingredients of chinese medicines have presented obvious efficacies in clinical treatment. Therefore, based on chinese medicine theory, we provide some ideas of screening agents for combination treatment of chinese medicines and MSC for ischemic stroke, and summarize the potentials of chinese medicines in MSC treatment and analyze the feasibilities of chinese medicines against side effects of MSC therapy. Consequently, we propose chinese medicines combing with MSC should be a promising approach to clinical stroke treatment in future.

关键词： chinese medicines combination treatment ischemic stroke mesenchymal stem cell

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Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin

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Neural Regeneration research 2025年第5期20卷 1445-1454页

作者： Meifeng Zheng Borui Zhang Sonata S Y Yau Kwok-Fai So Li Zhang Haining Ou Department of Rehabilitation medicine Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina Department of Rehabilitation medicine The Fifth Clinical College of Guangzhou Medical UniversityGuangzhouGuangdong ProvinceChina key laboratory of CNS Regeneration(Ministry of Education) Guangdong-Hong Kong-Macao Institute of CNS RegenerationJinan UniversityGuangzhouGuangdong ProvinceChina Department of Rehabilitation Sciences The Hong Kong Polytechnic UniversityHong Kong Special Administrative RegionChina state key laboratory of Brain and Cognitive Science Li Ka Shing Faculty of MedicineThe University of Hong KongHong Kong Special Administrative RegionChina Center for Exercise and Brain Science School of PsychologyShanghai University of SportShanghaiChina Neuroscience and Neurorehabilitation Institute University of Health and Rehabilitation SciencesQingdaoShandong ProvinceChina

Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug *** exercise enhances neurogenesis and synaptogenesis,and has been widely used for functional rehabilitation after *** this study,we determined whether exercise training before disease onset can alleviate the severity of cerebral *** also examined the role of exercise-induced circulating factors in these *** mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery *** found that this exercise pre-conditioning strategy effectively attenuated brain infarct area,inhibited gliogenesis,protected synaptic proteins,and improved novel object and spatial memory *** analysis showed that circulating adiponectin plays a critical role in these preventive effects of *** activation of adiponectin receptors by Adipo Ron mimicked the effects of exercise,while inhibiting receptor activation abolished the exercise *** summary,our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

关键词： adiponectin cerebral ischemia exercise pre-conditioning hippocampus memory function middle cerebral artery occlusion prefrontal cortex synaptic proteins treadmill exercise

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载体辅助免疫刺激剂通过下调PD-L1和抑制ATP水解增强光动力免疫治疗（英文）

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Science China Materials 2025年

作者：岑怡陈颖蔡华李欣璇陈霞云刘倩倩俞白雪刘已斌王涛李仕颖 The Fifth Affiliated Hospital Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology the NMPA and State Key Laboratory of Respiratory Disease the School of Pharmaceutical Sciences Guangzhou Medical University Graduate School Guangzhou University of Chinese Medicine Department of Pulmonary and Critical Care medicine Zhujiang Hospital Southern Medical University

肿瘤细胞存在免疫逃避和免疫抑制特性,极大削弱了免疫激活效应和抗肿瘤免疫疗效.本文开发了一种载体辅助免疫刺激剂(称为CoCeC),通过下调肿瘤细胞程序性死亡配体1 (PD-L1)和抑制三磷酸腺苷(ATP)水解,实现肿瘤光动力免疫治疗.其中,交联...

肿瘤细胞存在免疫逃避和免疫抑制特性,极大削弱了免疫激活效应和抗肿瘤免疫疗效.本文开发了一种载体辅助免疫刺激剂(称为CoCeC),通过下调肿瘤细胞程序性死亡配体1 (PD-L1)和抑制三磷酸腺苷(ATP)水解,实现肿瘤光动力免疫治疗.其中,交联的寡聚壳聚糖是递送二氢卟吩e6和色瑞替尼的药物载体,也是下调PD-L1的免疫佐剂,可抑制肿瘤细胞的免疫逃逸.同时, CoCeC的光动力疗法(PDT)能破坏肿瘤细胞,进而诱导肿瘤细胞发生免疫原性死亡(ICD)并释放损伤相关分子模式(DAMPs),阻断CD39抑制ATP水解为腺苷,从而抑制腺苷造成的肿瘤免疫抑制特性.体外和体内研究结果表明, CoCeC能有效抑制原发性肿瘤的生长,并通过改善肿瘤免疫原性、阻断肿瘤免疫逃逸和逆转肿瘤免疫抑制特性,实现光动力免疫激活和肺转移瘤免疫治疗的目的.这种载体自佐剂策略为纳米药物理性设计提供了新方法,并为逆转多重肿瘤免疫抑制特性和激活抗肿瘤免疫治疗提供了新思路.

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Hypaconitine inhibits TGF-β1-induced epithelial–mesenchymal transition and suppresses adhesion,migration,and invasion of lung cancer A549 cells

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chinese Journal of Natural medicines 2017年第6期15卷 427-435页

作者： FENG Hai-Tao ZHAO Wen-Wen LU Jin-Jian WANG Yi-Tao CHEN Xiu-Ping state key laboratory of quality research in chinese medicine Institute of Chinese Medical Sciences University of MacaoMacao China

Epithelial-mesenchymal transition(EMT) has been implicated in tumor invasion and metastasis and provides novel strategies for cancer therapy. Hypaconitine(HpA), a diester-diterpenoid alkaloid isolated from the root of the Aconitum species, exhibits anti-inflammatory, analgesic, and especially, cardiotoxic activities. Here, we reported the anti-metastatic potentials of HpA in transforming growth factor-β1(TGF-β1)-induced EMT in lung cancer A549 cells. The cytotoxic effect of HpA was determined by MTT assay. A549 cells were treated with TGF-β1 with or without HpA co-treatment, and the morphological alterations were observed with a microscopy. The expression of E-cadherin, N-cadherin, and NF-κB was determined by both Western blotting and immunofluorescence analyses. The adhesion, migration, and invasion were detected with Matrigel, wound-healing, and transwell assays, respectively. The expression of Snail was determined by Western blotting. The expression of NF-κB p65, IκBα, and p-IκBα in nuclear and cytosolic extracts was assessed by Western blotting. The results showed that low concentration of HpA(<16 μmol×L^(–1)) had no obvious cytotoxicity to A549 cells. Morphologically, TGF-β1 treatment induced spindle-shaped alteration in the cells. The upregulation of N-cadherin, NF-κB, and Snail and the downregulation of E-cadherin were detected after TGF-β1 treatment. The adhesion, migration and invasion abilities were also increased by TGF-β1. Besides, TGF-β1 induced expression of Snail in a time-dependent manner. Furthermore, TGF-β1 induced nuclear translocation of NF-κB p65. All these alterations were dramatically inhibited by HpA co-treatment. In addition, the NF-κB inhibitor PDTC showed similar inhibitory effect. In conclusion, these results showed that HpA inhibited TGF-β1-induced EMT in A549 cells, which was possibly mediated by the inactivation of the NF-κB signaling pathway, providing an evidence for anti-cancer effect of HpA.

关键词： EMT Hypaconitine TGF-β1 NF-κB

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Preparation and characterization of pelletized solid dispersion of resveratrol with mesoporous silica microparticles to improve dissolution by fluid-bed coating techniques

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Asian Journal of Pharmaceutical Sciences 2016年第4期11卷 528-535页

作者： Jian Li Xiaoqing Miao Tongkai Chen Defang Ouyang Ying Zheng state key laboratory of quality research in chinese medicine Institute of Chinese Medical Sciences University of Macao

With hydrophilic surface and high surface area, porous silica has been applied to load insoluble drugs. Compared to solvent equilibrium method, resveratrol(RES)–mesoporous silica microparticles(MSM) solid dispersion prepared by fluid bed demonstrated higher drug loading and more complete dissolution. Pore volume and diameter have more remarkable effects than surface area to the drug loading and in vitro dissolution profiles. RES–polyethylene glycol solid dispersion with high drug loading showed fast but incomplete dissolution due to the recrystallization. The combination of fluid bed and MSM was an effective strategy to improve drug loading as well as dissolution for poorly water-soluble drugs.

关键词： Resveratrol (RES) Solid dispersion Mesoporous silica microparticles (MSM) Fluid bed Amorphous

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Using induced pluripotent stem cells for modeling Parkinson’s disease

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World Journal of Stem Cells 2019年第9期11卷 634-649页

作者： Minjing Ke Cheong-Meng Chong Huanxing Su state key laboratory of quality research in chinese medicine Institute of Chinese Medical Sciences University of Macao

Parkinson’s disease(PD)is an age-related neurodegenerative disease caused by the progressive loss of dopaminergic(DA)neurons in the substantia *** DA neurons degenerate,PD patients gradually lose their ability of *** date no effective therapies are available for the treatment of PD and its pathogenesis remains *** models that appropriately mimic the development of PD are certainly needed for gaining mechanistic insights into PD pathogenesis and identifying new therapeutic *** induced pluripotent stem cells(iPSCs)could provide a promising model for fundamental research and drug *** this review,we summarize various iPSCs-based PD models either derived from PD patients through reprogramming technology or established by gene-editing technology,and the promising application of iPSC-based PD models for mechanistic studies and drug testing.

关键词： Parkinson’s disease Dopaminergic neurons Induced pluripotent stem cells Somatic cell reprogramming Aging

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Investigating the molecular dissolution process of binary solid dispersions by molecular dynamics simulations

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Asian Journal of Pharmaceutical Sciences 2018年第3期13卷 248-254页

作者： TengIan Chan Defang Ouyang state key laboratory of quality research in chinese medicine Institute of Chinese Medical Sciences University of Macao

Dissolution molecular mechanism of solid dispersions still remains unclear despite thousands of reports about this technique. The aim of current research was to investigate the molecular dissolution mechanism of solid dispersions by molecular dynamics simulations. The formation of ibuprofen/polymer solid dispersions was modeled by the simulated annealing method. After that, the models of solid dispersions were immersed into the water box with 25–30 ? thicknesses and 50–100 ns MD simulations were performed to all *** results showed various dissolution behaviors in different particle sizes and various polymers of solid dispersions. Small-sized particles of solid dispersions dissolved quickly in the water, while the large particles of PEG or PVP-containing solid dispersions gradually swelled in the dissolution process and drug molecules may aggregate together. In the dissolution process, the carboxylic groups of ibuprofen molecules turned its direction from polymer molecules to external water box and then the drug molecules left the polymer *** the same time, polymer coils gradually relaxed and became free polymer chains in the solution. In addition, solid dispersion with poloxamer could prevent the precipitate of drug molecules in the dissolution process, which is different from those of PEG or PVPcontaining systems. This research provided us clear images of dissolution process of solid dispersions at the molecular level.

关键词： Solid dispersion Molecular modeling Dissolution process Ibuprofen

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Ginsenoside Rk2, a dehydroprotopanaxadiol saponin, alleviates alcoholic liver disease via regulating NLRP3 and NLRP6 inflammasome signaling pathways in mice

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Journal of Pharmaceutical Analysis 2023年第9期13卷 999-1012页

作者： Jian Zou Rujie Yang Ruibing Feng Jiayue Liu Jian-Bo Wan state key laboratory of quality research in chinese medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao SARChina

Heavy alcohol consumption results in alcoholic liver disease(ALD)with inadequate therapeutic ***,we first report the potential beneficial effects of ginsenoside Rk2(Rk2),a rare dehydroprotopanaxadiol saponin isolated from streamed ginseng,against alcoholic liver injury in ***-plus-single-binge ethanol feeding caused severe liver injury,as manifested by significantly elevated serum aminotransferase levels,hepatic histological changes,increased lipid accumulation,oxidative stress,and inflammation in the *** deleterious effects were alleviated by the treatment with Rk2(5 and 30 mg/kg).Acting as an nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3(NLRP3)inhibitor,Rk2 ameliorates alcohol-induced liver inflammation by inhibiting NLRP3 inflammasome signaling in the ***,the treatment with Rk2 alleviated the alcohol-induced intestinal barrier dysfunction via enhancing NLRP6 inflammasome in the *** findings indicate that Rk2 is a promising agent for the prevention and treatment of ALD and other NLPR3-driven diseases.

关键词： Alcoholic liver disease Ginsenoside Rk2 NLRP3 inflammasome NLRP6 inflammasome Intestinal barrier dysfunction

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Microneedle-assisted dual delivery of PUMA gene and celastrol for synergistic therapy of rheumatoid arthritis through restoring synovial homeostasis

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Bioactive Materials 2024年第6期36卷 83-95页

作者： Peng Hua Ruifeng Liang Suleixin Yang Yanbei Tu Meiwan Chen state key laboratory of quality research in chinese medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao SARChina

Abnormal proliferation of aggressive fibroblast-like synoviocytes(FLS)and perpetuate synovial inflammation can inevitably accelerate the progression of rheumatoid arthritis(RA).Herein,a strategy of simultaneously promoting FLS apoptosis and inhibiting inflammation as mediated by macrophages is proposed to restore synovial homeostasis for effective RA therapy.A hyaluronic acid-based dissolvable microneedle(MN)is fabricated for transdermal delivery of dual human serum albumin(HSA)-contained biomimetic nanocomplexes to regulate RA FLS and *** skin insertion,dual nanocomplexes are released rapidly from the MN and accumulate in RA joint microenvironment through both passive and active targeting as mediated by ***-crosslinked fluorinated polyethyleneimine 1.8 K(^(TK)PF)was constructed to bind the plasmid encoding pro-apoptotic gene PUMA with HSA coating layer(^(TK)PF/pPUMA@HSA,TPH).TPH nanocomplexes can upregulate PUMA through RA FLS transfection to trigger efficient ***,HSA nanocomplexes encapsulating the classic anti-inflammatory natural product celastrol(Cel@HSA,CH)can inhibit inflammation of macrophages through blocking NF-κB pathway ***/CH MN can deplete RA FLS and inhibit M1 macrophage activation,suppress synovial hyperplasia as well as reduce bone and cartilage erosion in a collagen-induced arthritis(CIA)mouse model,demonstrating a promising strategy for efficient RA treatment.

关键词： Rheumatoid arthritis PUMA Celastrol Anti-inflammation Fibroblast-like synoviocyte apoptosis

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